Publications by authors named "Alba M Garcia-Serrano"

Hypothalamic inflammation underlies diet-induced obesity and diabetes in rodent models. While diet normalization largely allows for recovery from metabolic impairment, it remains unknown whether long-term hypothalamic inflammation induced by obesogenic diets is a reversible process. In this study, we aimed at determining sex specificity of hypothalamic neuroinflammation and gliosis in mice fed a fat- and sugar-rich diet, and their reversibility upon diet normalization.

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Excess dietary salt reduces resting cerebral blood flow (CBF) and vascular reactivity, which can limit the fueling of neuronal metabolism. It is hitherto unknown whether metabolic derangements induced by high-salt-diet (HSD) exposure during adulthood are reversed by reducing salt intake. In this study, male and female mice were fed an HSD from 9 to 16 months of age, followed by a normal-salt diet (ND) thereafter until 23 months of age.

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Obesity constitutes a risk factor for cognitive impairment. In rodent models, long-term exposure to obesogenic diets leads to hippocampal taurine accumulation. Since taurine has putative cyto-protective effects, hippocampal taurine accumulation in obese and diabetic models might constitute a counteracting response to metabolic stress.

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Obesity, type 2 diabetes, and their associated comorbidities impact brain metabolism and function and constitute risk factors for cognitive impairment. Alterations to taurine homeostasis can impact a number of biological processes, such as osmolarity control, calcium homeostasis, and inhibitory neurotransmission, and have been reported in both metabolic and neurodegenerative disorders. Models of neurodegenerative disorders show reduced brain taurine concentrations.

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Diabetes impacts on brain metabolism, structure, and function. Alterations in brain metabolism have been observed in obesity and diabetes models induced by exposure to diets rich in saturated fat and/or sugar and have been linked to memory impairment. However, it remains to be determined whether brain dysfunction induced by obesogenic diets results from permanent brain alterations.

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The hypothalamus is the central regulator of energy homeostasis. Hypothalamic neuronal circuits are disrupted upon overfeeding, and play a role in the development of metabolic disorders. While mouse models have been extensively employed for understanding the mechanisms of hypothalamic dysfunction, functional magnetic resonance imaging (fMRI) on hypothalamic nuclei has been challenging.

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Article Synopsis
  • - Type 2 diabetes (T2D) negatively affects brain function through issues like glucose toxicity, blood-brain barrier damage, and oxidative stress, leading to problems in memory and cognitive processes.
  • - Research using rodent models, particularly mice and rats fed high-fat or high-sugar diets, has helped reveal how T2D contributes to brain dysfunction, especially impacting hippocampal-related tasks.
  • - The article summarizes key discoveries about how metabolic syndrome caused by unhealthy diets alters brain energy metabolism, affecting both neurons and supporting glial cells, ultimately leading to a T2D phenotype.
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Article Synopsis
  • Diabetes negatively affects cognitive function by impairing brain glycogen metabolism, which is essential for neuronal activity and memory.
  • A study using magnetic resonance spectroscopy found that glucose incorporation into brain glycogen was significantly lower in type 2 diabetic rats (GK rats) compared to healthy control rats (Wistar rats).
  • Type 2 diabetes also reduced glucose transport and utilization in the brain, especially affecting regions like the hippocampus, which is critical for memory, and the hypothalamus, involved in energy regulation.
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